The Yogi masters were right -- meditation and breathing exercises can sharpen your mind

New research explains link between breath-focused meditation and attention and brain health

May 10, 2018

Science Daily/Trinity College Dublin

It has long been claimed by Yogis and Buddhists that meditation and ancient breath-focused practices, such as pranayama, strengthen our ability to focus on tasks. A new study explains for the first time the neurophysiological link between breathing and attention.

Breath-focused meditation and yogic breathing practices have numerous known cognitive benefits, including increased ability to focus, decreased mind wandering, improved arousal levels, more positive emotions, decreased emotional reactivity, along with many others. To date, however, no direct neurophysiological link between respiration and cognition has been suggested.

The research shows for the first time that breathing -- a key element of meditation and mindfulness practices -- directly affects the levels of a natural chemical messenger in the brain called noradrenaline. This chemical messenger is released when we are challenged, curious, exercised, focused or emotionally aroused, and, if produced at the right levels, helps the brain grow new connections, like a brain fertiliser. The way we breathe, in other words, directly affects the chemistry of our brains in a way that can enhance our attention and improve our brain health.

The study, carried out by researchers at Trinity College Institute of Neuroscience and the Global Brain Health Institute at Trinity, found that participants who focused well while undertaking a task that demanded a lot of attention had greater synchronisation between their breathing patterns and their attention, than those who had poor focus. The authors believe that it may be possible to use breath-control practices to stabilise attention and boost brain health.

Michael Melnychuk, PhD candidate at the Trinity College Institute of Neuroscience, Trinity, and lead author of the study, explained: "Practitioners of yoga have claimed for some 2,500 years, that respiration influences the mind. In our study we looked for a neurophysiological link that could help explain these claims by measuring breathing, reaction time, and brain activity in a small area in the brainstem called the locus coeruleus, where noradrenaline is made. Noradrenaline is an all-purpose action system in the brain. When we are stressed we produce too much noradrenaline and we can't focus. When we feel sluggish, we produce too little and again, we can't focus. There is a sweet spot of noradrenaline in which our emotions, thinking and memory are much clearer."

"This study has shown that as you breathe in locus coeruleus activity is increasing slightly, and as you breathe out it decreases. Put simply this means that our attention is influenced by our breath and that it rises and falls with the cycle of respiration. It is possible that by focusing on and regulating your breathing you can optimise your attention level and likewise, by focusing on your attention level, your breathing becomes more synchronised."

The research provides deeper scientific understanding of the neurophysiological mechanisms which underlie ancient meditation practices. The findings were recently published in a paper entitled 'Coupling of respiration and attention via the locus coeruleus: Effects of meditation and pranayama' in the journal Psychophysiology. Further research could help with the development of non-pharmacological therapies for people with attention compromised conditions such as ADHD and traumatic brain injury and in supporting cognition in older people.

There are traditionally two types of breath-focused practices -- those that emphasise focus on breathing (mindfulness), and those that require breathing to be controlled (deep breathing practices such as pranayama). In cases when a person's attention is compromised, practices which emphasise concentration and focus, such as mindfulness, where the individual focuses on feeling the sensations of respiration but make no effort to control them, could possibly be most beneficial. In cases where a person's level of arousal is the cause of poor attention, for example drowsiness while driving, a pounding heart during an exam, or during a panic attack, it should be possible to alter the level of arousal in the body by controlling breathing. Both of these techniques have been shown to be effective in both the short and the long term.

Ian Robertson, Co-Director of the Global Brain Health Institute at Trinity and Principal Investigator of the study added: "Yogis and Buddhist practitioners have long considered the breath an especially suitable object for meditation. It is believed that by observing the breath, and regulating it in precise ways -- a practice known as pranayama -- changes in arousal, attention, and emotional control that can be of great benefit to the meditator are realised. Our research finds that there is evidence to support the view that there is a strong connection between breath-centred practices and a steadiness of mind."

"Our findings could have particular implications for research into brain ageing. Brains typically lose mass as they age, but less so in the brains of long term meditators. More 'youthful' brains have a reduced risk of dementia and mindfulness meditation techniques actually strengthen brain networks. Our research offers one possible reason for this -- using our breath to control one of the brain's natural chemical messengers, noradrenaline, which in the right 'dose' helps the brain grow new connections between cells. This study provides one more reason for everyone to boost the health of their brain using a whole range of activities ranging from aerobic exercise to mindfulness meditation."

https://www.sciencedaily.com/releases/2018/05/180510101254.htm

Depression linked to memory problems and brain aging

May 9, 2018

Science Daily/American Academy of Neurology

Depression in older adults may be linked to memory problems, according to new research. The study also showed that older people with greater symptoms of depression may have structural differences in the brain compared to people without symptoms.

"Since symptoms of depression can be treated, it may be possible that treatment may also reduce thinking and memory problems," said study author Adina Zeki Al Hazzouri, PhD, MS, of the University of Miami Miller School of Medicine in Florida. "With as many as 25 percent of older adults experiencing symptoms of depression, it's important to better understand the relationship between depression and memory problems."

The study involved 1,111 people who were all stroke-free with an average age of 71. The majority were Caribbean Hispanic. At the beginning of the study, all had brain scans, a psychological exam and assessments for memory and thinking skills. Their memory and thinking skills were tested again an average of five years later.

At the start of the study, 22 percent of participants had greater symptoms of depression. This was defined as a score of 16 or higher on a test with a range of 0-60, which is considered at risk for clinical depression. For the test, participants reported how often in the past week they agreed with statements such as "I was bothered by things that usually don't bother me" and "I did not feel like eating." Researchers found after adjusting for age, race, anti-depressive medications, and other variables, greater symptoms of depression were linked to worse episodic memory. Scores on tests were lower by 0.21 of a standard deviation compared to those without greater symptoms of depression. Episodic memory is a person's ability to remember specific experiences and events.

Researchers also found those with greater symptoms of depression had differences in the brain including smaller brain volume as well as a 55 percent greater chance of small vascular lesions in the brain.

Researchers found no evidence of a relationship between greater symptoms of depression and changes in thinking skills over five years.

"Small vascular lesions in the brain are markers of small vessel disease, a condition in which the walls in the small blood vessels are damaged," said Zeki Al Hazzouri. "Our research suggests that depression and brain aging may occur simultaneously, and greater symptoms of depression may affect brain health through small vessel disease."

Zeki Al Hazzouri noted that the study provides information about depression and memory and thinking skills, especially among people who identified as Hispanic, who have been insufficiently studied in previous studies on the topic, even though they can be at increased risk of dementia in late life.

Limitations of the study include that participants had to be healthy enough to have an MRI, so they may have been healthier than the general population. Also, the study was over a five-year period, which may not have been long enough to capture meaningful changes in thinking and memory abilities over time.

https://www.sciencedaily.com/releases/2018/05/180509162704.htm

Researchers discover connection between circadian rhythm and aggression

May 2, 2018

Science Daily/University of Copenhagen The Faculty of Health and Medical Sciences

A research team has discovered a circuit in the brains of mice connecting circadian rhythm to aggressive behavior. The discovery is particularly interesting to Alzheimer's patients who experience increased aggression at night. The researchers have developed special protein tools capable of turning off the cells in the brain causing the behavior.

Each year around many people worldwide are diagnosed with a form of dementia. Alzheimer's disease is one of them. The disease manifests itself in memory difficulties in particular, but can also result in personality changes and mood swings.

When the sun sets 20 per cent of all Alzheimer's patients experience increased bewilderment, anxiety, unease, disorientation, irritation and aggression. This phenomenon is called 'sundowning' or sundown syndrome. At worst, the condition can mean that the patient must be left in professional care, as it can be difficult for family members to handle. The cause of the condition is unknown, but previous research has suggested that it is connected to the circadian rhythm.

A research team including a researcher from the Department of Drug Design and Pharmacology at the University of Copenhagen is now able to confirm this connection. The researchers have identified and mapped a circuit between the part of the brain containing the circadian clock or circadian rhythm and a part of the brain controlling aggression.

'We have shown that the circadian clock in mice is closely linked to an aggression centre in the mouse brain by a cell circuit. The human brain has those same groups of cells that the circuit goes through. With this knowledge, we are now enabled to target this circuit pharmacologically and target cells that make people aggressive at the end of the day', says Assistant Professor Timothy Lynagh from the Department of Drug Design and Pharmacology at the University of Copenhagen.

Turn off the Aggression

The inner clock or circadian rhythm is located in the part of the brain called suprachiasmatic nucleus. One of the parts of the brain that control aggressive behaviour is called the ventromedial hypothalamus. Researchers have previously observed a connection between the two parts of the brain, though none have had knowledge of the specific circuit connecting them.

Using electrophysiology and microscopy, the researchers measured the activity of the brain cells at main author Clifford Saper's laboratory in Boston. They also turned off parts of the cell circuit in the brains of mice to map the circuit and to identify the cells connecting the two parts of the brain. To map circuits in the brain you need a protein tool that can turn off the various cells to determine their function. Assistant Professor Timothy Lynagh has designed precisely such a tool.

'We take a receptor and mutate it, so that it is not sensitive to anything in the brain, but very sensitive to a particular drug. The tool works like an on/off switch. When you put the protein tool in the mouse brain, under normal circumstances, nothing will happen. But when you give the animal the drug, the cells that have the receptor on them will be turned off', Timothy Lynagh explains.

Using this tool, the researchers can thus in theory turn off the cells that cause people suffering from sundown syndrome to become more aggressive at night.

May Be Used on Humans 20 Years into the Future

The tool can also be used in other contexts than sundown syndrome. In other studies, Tim Lynagh's tool has been used to turn off cells in rats linked to anxiety and fear.

'If you can start understanding which cells in the brain lead to which problems, you can then put this tool into any of those parts of the brain. The person who takes the drug will then have the cells causing the problem turned off', Timothy Lynagh says.

Even though the study was conducted on mice, the tool and the knowledge the research has generated can potentially be used in the treatment of humans.

'Because of the huge advances that are coming along with CRISPR, I would be tempted to say that based on a recent demonstration of gene therapy for brain disease, potentially, it could be used in the human brain in 20 years' time. Of course it needs a lot more research', he says.

https://www.sciencedaily.com/releases/2018/05/180502104100.htm

Music activates regions of the brain spared by Alzheimer's disease

April 28, 2018

Science Daily/University of Utah Health

Researchers are looking to the salience network of the brain to develop music-based treatments to help alleviate anxiety in patients with dementia.

Ever get chills listening to a particularly moving piece of music? You can thank the salience network of the brain for that emotional joint. Surprisingly, this region also remains an island of remembrance that is spared from the ravages of Alzheimer's disease. Researchers at the University of Utah Health are looking to this region of the brain to develop music-based treatments to help alleviate anxiety in patients with dementia. Their research will appear in the April online issue of The Journal of Prevention of Alzheimer's Disease.

"People with dementia are confronted by a world that is unfamiliar to them, which causes disorientation and anxiety" said Jeff Anderson, M.D., Ph.D., associate professor in Radiology at U of U Health and contributing author on the study. "We believe music will tap into the salience network of the brain that is still relatively functioning."

Previous work demonstrated the effect of a personalized music program on mood for dementia patients. This study set out to examine a mechanism that activates the attentional network in the salience region of the brain. The results offer a new way to approach anxiety, depression and agitation in patients with dementia. Activation of neighboring regions of the brain may also offer opportunities to delay the continued decline caused by the disease.

For three weeks, the researchers helped participants select meaningful songs and trained the patient and caregiver on how to use a portable media player loaded with the self-selected collection of music.

"When you put headphones on dementia patients and play familiar music, they come alive," said Jace King, a graduate student in the Brain Network Lab and first author on the paper. "Music is like an anchor, grounding the patient back in reality."

Using a functional MRI, the researchers scanned the patients to image the regions of the brain that lit up when they listened to 20-second clips of music versus silence. The researchers played eight clips of music from the patient's music collection, eight clips of the same music played in reverse and eight blocks of silence. The researchers compared the images from each scan.

The researchers found that music activates the brain, causing whole regions to communicate. By listening to the personal soundtrack, the visual network, the salience network, the executive network and the cerebellar and corticocerebellar network pairs all showed significantly higher functional connectivity.

"This is objective evidence from brain imaging that shows personally meaningful music is an alternative route for communicating with patients who have Alzheimer's disease," said Norman Foster, M.D., Director of the Center for Alzheimer's Care at U of U Health and senior author on the paper. "Language and visual memory pathways are damaged early as the disease progresses, but personalized music programs can activate the brain, especially for patients who are losing contact with their environment."

However, these results are by no means conclusive. The researchers note the small sample size (17 participants) for this study. In addition, the study only included a single imaging session for each patient. It is remains unclear whether the effects identified in this study persist beyond a brief period of stimulation or whether other areas of memory or mood are enhanced by changes in neural activation and connectivity for the long term.

"In our society, the diagnoses of dementia are snowballing and are taxing resources to the max," Anderson said. "No one says playing music will be a cure for Alzheimer's disease, but it might make the symptoms more manageable, decrease the cost of care and improve a patient's quality of life."

https://www.sciencedaily.com/releases/2018/04/180428145111.htm

Vitamin B6 helps people recall their dreams

April 27, 2018

Science Daily/University of Adelaide

New research has found that taking vitamin B6 could help people to recall their dreams.

The study published online ahead of print in Perceptual and Motor Skills, included 100 participants from around Australia taking high-dose vitamin B6 supplements before going to bed for five consecutive days.

"Our results show that taking vitamin B6 improved people's ability to recall dreams compared to a placebo," says research author Dr Denholm Aspy, from the University's School of Psychology.

"Vitamin B6 did not affect the vividness, bizarreness or colour of their dreams, and did not affect other aspects of their sleep patterns.

"This is the first time that such a study into the effects of vitamin B6 and other B vitamins on dreams has been carried out on a large and diverse group of people," Dr Aspy says.

The randomised, double-blind, placebo-controlled study saw participants taking 240mg of vitamin B6 immediately before bed.

Prior to taking the supplements, many of the participants rarely remembered their dreams, but they reported improvements by the end of the study.

"It seems as time went on my dreams were clearer and clearer and easier to remember. I also did not lose fragments as the day went on," said one of the participants after completing the study.

According to another participant of the study, "My dreams were more real, I couldn't wait to go to bed and dream!"

Dr Aspy says: "The average person spends around six years of their lives dreaming. If we are able to become lucid and control our dreams, we can then use our dreaming time more productively.

"Lucid dreaming, where you know that you are dreaming while the dream is still happening, has many potential benefits. For example, it may be possible to use lucid dreaming for overcoming nightmares, treating phobias, creative problem solving, refining motor skills and even helping with rehabilitation from physical trauma.

"In order to have lucid dreams it is very important to first be able to recall dreams on a regular basis. This study suggests that vitamin B6 may be one way to help people have lucid dreams."

Vitamin B6 occurs naturally in various foods, including whole grain cereals, legumes, fruits (such as banana and avocado), vegetables (such as spinach and potato), milk, cheese, eggs, red meat, liver, and fish.

"Further research is needed to investigate whether the effects of vitamin B6 vary according to how much is obtained from the diet. If vitamin B6 is only effective for people with low dietary intake, its effects on dreaming may diminish with prolonged supplementation," says Dr Aspy.

https://www.sciencedaily.com/releases/2018/04/180427100258.htm

Loss of brain synchrony may explain working memory limits

April 26, 2018

Science Daily/City University London

A new study may have revealed the reasons behind our memory limitations. The researchers found that trying to retain too much information in our working memory leads to a communication breakdown between parts of the brain responsible for maintaining it.

Everyday experience makes it obvious -- sometimes frustratingly so -- that our working memory capacity is limited and we can only keep so many things consciously in mind at once. The results of a new study, which is published in the journal Cerebral Cortex, may explain why: The authors suggest that the 'coupling', or synchrony, of brain waves among three key regions breaks down in specific ways when visual working memory load becomes too much to handle. This loss of synchrony means the regions can no longer communicate with each other to sustain working memory.

Maximum working memory capacity -- for instance the total number of images a person can hold in working memory at the same time -- varies between individuals but averages about seven. This new study tries to understand what causes the memory to have this intrinsic limit.

The study's lead author, Dr Dimitris Pinotsis, a lecturer at the Department of Psychology at City, University of London, and a research affiliate at the Department of Brain and Cognitive Sciences at MIT, said: "At peak memory capacity, the brain signals that maintain memories and guide actions based on these memories, reach their maximum. Above this peak, the same signals break down."

As researchers have previously correlated working memory capacity with intelligence, understanding what causes working memory to have an intrinsic limit is important because it could also help explain the limited nature of conscious thought and how it might break down in diseases.

"Because certain psychiatric diseases can lower capacity, the findings could explain more about how such diseases interfere with thinking," said Professor Earl Miller, the study's senior author and the Picower Professor of Neuroscience at MIT's Picower Institute for Learning and Memory. The study's other author is Dr Timothy Buschman, assistant professor at the Princeton University Neuroscience Institute.

To investigate working memory limits, the researchers carried out a detailed statistical analysis of data when animal subjects played a simple game. They had to spot the difference when they were shown a set of squares on a screen and then, after a brief blank screen, a nearly identical set in which one square had changed colour. The number of squares involved, hence the working memory load of each round, varied so that sometimes the task exceeded the animals' capacity.

As the animals played, the researchers measured the frequency and timing of brain waves produced by ensembles of neurons in three regions presumed to have an important -- though as yet unknown -- relationship in producing visual working memory: the prefrontal cortex (PFC), the frontal eye fields (FEF), and the lateral intraparietal area (LIP).

Using sophisticated mathematical techniques, they found that the regions essentially work as a committee, without much hierarchy, to keep working memory going. They also found changes as working memory approached and then exceeded capacity. In particular, the researchers found that above capacity the PFC's coupling to the FEF and LIP at low frequency stopped.

As previous studies have suggested that the PFC's role might be to employ low-frequency waves to provide the feedback the keeps the working memory system in sync, the researchers suggest that when that signal breaks down, the whole enterprise may as well. This observation may also explain why memory capacity has a finite limit.

Professor Miller said: "We knew that stimulus load degrades stimulus processing in various brain areas, but we hadn't seen any distinct change that correlated with reaching capacity, but we did see this with feedback coupling. It drops off when the subjects exceeded their capacity. The PFC stops providing feedback coupling to the FEF and LIP."

The findings could also help optimise heads-up displays in cars and to develop diagnostic tests for diseases like schizophrenia and dementia, among other applications.

"Understanding brain signals at peak load can help us understand the origins of cognitive impairments. This could lead to new therapeutic approaches for people in need, like schizophrenics," said Dr Pinotsis.

The US National Institute of Mental Health and the MIT's Picower Institute Innovation Fund supported this study.

https://www.sciencedaily.com/releases/2018/04/180426110502.htm

Antidepressants and bladder medicines linked to dementia in landmark study

April 25, 2018

Science Daily/University of East Anglia

Long-term use of some anticholinergic medications are associated with an increased risk of dementia, according to a new study.

Anticholinergic antidepressants have been found to be linked with dementia, even when taken up to 20 years before a diagnosis.

The research, funded by Alzheimer's Society and published today in the BMJ, also shows a dementia risk associated with medications prescribed for bladder conditions and Parkinson's.

However several other anticholinergic medications, including anti-histamines and those used for abdominal cramps, were not found to be linked to dementia -- despite previous research suggesting that any anticholinergic might represent a risk.

Anticholinergic drugs are used to treat a variety of conditions and work by blocking a key messenger (neurotransmitter) in the body called acetylcholine.

The research team studied the medical records of 40,770 patients aged over 65 diagnosed with dementia, and compared them to the records of 283,933 people without dementia. More than 27 million prescriptions were analysed.

This is the largest and most detailed study of its kind into the long-term impact of anticholinergic use in relation to dementia.

The team drilled down to see whether there were links between different classes of anticholinergic medication and incidence of dementia diagnosis.

They found that there was a greater incidence of dementia among patients prescribed greater quantities of anticholinergic antidepressants, and anticholinergic medication for bladder conditions and Parkinson's.

The link between these medications and dementia cannot tell us that they are directly causing the condition, but this work does suggests a potential preventative approach to reduce dementia which is a priority.

The study concludes that clinicians should consider long-term anti-cholinergic effects when prescribing.

Patients with concerns should continue taking their medicines until they have consulted their doctor or pharmacist.

Lead researcher Dr George Savva from UEA's School of Health Sciences said: "More than 50 million people worldwide are affected by dementia and this number is estimated to be 132 million by 2050. Developing strategies to prevent dementia is therefore a global priority.

"We studied patients with a new dementia diagnosis and looked at what anticholinergic medication they were prescribed between four and 20 years prior to being diagnosed.

"We found that people who had been diagnosed with dementia were up to 30 per cent more likely to have been prescribed specific classes of anticholinergic medications. And the association with dementia increases with greater exposure to these types of medication.

"What we don't know for sure is whether the medication is the cause. It could be that these medications are being prescribed for very early symptoms indicating the onset of dementia.

"But because our research shows that the link goes back up to 15 or 20 years before someone is eventually diagnosed with dementia, it suggests that reverse causation, or confounding with early dementia symptoms, probably isn't the case.

"This research is really important because there are an estimated 350 million people affected globally by depression, and bladder conditions requiring treatment are estimated to affect over 13 per cent of men and 30 per cent of women in the UK and US.

"Many of the treatment options for these conditions involve medication with anticholinergic effects.

Dr Doug Brown, Chief Policy and Research Officer at Alzheimer's Society, said: "This large study confirms that some anticholinergic drugs can raise the risk of dementia -- but it should also put minds at ease as there appears to be no dementia risk with anticholinergic drugs used to treat common conditions like hayfever, travel sickness and stomach cramps.

"Current guidelines for doctors say that anticholinergic drugs should be avoided for frail older people because of their impact on memory and thinking, but doctors should consider these new findings for all over-65s as long-term use could raise the risk of dementia."

Dr Noll Campbell, a collaborator and co-author on the paper, said: "These results suggest we should prioritise safer alternatives to anticholinergic medications long before symptoms of dementia are recognised." Dr Campbell is an investigator with the Regenstrief Institute and Indiana University Center for Aging Research and is an assistant professor with Purdue University College of Pharmacy in the United States.

The study used data from Clinical Practice Research Datalink which includes anonymised diagnosis, referral and prescription records for more than 11 million patients from 674 primary care practices across the UK. The data is broadly representative of the UK population in terms of age, sex and ethnicity.

Prof Chris Fox, Professor of Clinical Psychiatry at UEA's Norwich Medical School and Consultant Psychiatrist, said: "While the associations are moderate, given the high incidence of dementia, they reflect a potentially important risk to patients.

"Doctors and patients should therefore be vigilant about using anticholinergic medications.

"They need to consider the risk of long-term cognitive effects, as well as short-term effects, associated with specific drugs when weighing up risks and benefits.

"We don't know exactly how anticholinergics might cause dementia. Further research is needed to understand possible reasons for this link. In the meantime, I strongly advise patients with any concerns to continue taking their medicines until they have consulted their doctor or pharmacist."

Dr Ian Maidment, Senior Lecturer in Clinical Pharmacy at Aston University and lead pharmacist on the study, said: "We already have strong evidence that anticholinergics cause confusion and in the short-term will potentially worsen the symptoms of dementia. Long-term data is more difficult to obtain, because clinical trials tend be short term.

"This study shows that some anticholinergics may cause long-term harm in addition to short-term harm.

"Other recent research has shown a dramatic increase in polypharmacy -- the number of older people taking five or more medicines has quadrupled over 20 years to nearly half of all older people.

"With many different medicines having at least some anticholinergic activity, one focus should be de-prescribing. Doctors, nurses and pharmacists need to work with older people and their carers to ensure that they only take medication if the benefits clearly outweigh the harms."

https://www.sciencedaily.com/releases/2018/04/180425195636.htm

Lack of sleep may be linked to risk factor for Alzheimer's disease

Preliminary study shows increased levels of beta-amyloid

April 13, 2018

Science Daily/NIH/National Institute on Alcohol Abuse and Alcoholism

Losing just one night of sleep led to an immediate increase in beta-amyloid, a protein in the brain associated with Alzheimer's disease, according to a small, new study.

While acute sleep deprivation is known to elevate brain beta-amyloid levels in mice, less is known about the impact of sleep deprivation on beta-amyloid accumulation in the human brain. The study is among the first to demonstrate that sleep may play an important role in human beta-amyloid clearance.

"This research provides new insight about the potentially harmful effects of a lack of sleep on the brain and has implications for better characterizing the pathology of Alzheimer's disease," said George F. Koob, Ph.D., director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health, which funded the study.

Beta-amyloid is a metabolic waste product present in the fluid between brain cells. In Alzheimer's disease, beta-amyloid clumps together to form amyloid plaques, negatively impacting communication between neurons.

Led by Drs. Ehsan Shokri-Kojori and Nora D. Volkow of the NIAAA Laboratory of Neuroimaging, the study is now online in the Proceedings of the National Academy of Sciences. Dr. Volkow is also the director of the National Institute on Drug Abuse at NIH.

To understand the possible link between beta-amyloid accumulation and sleep, the researchers used positron emission tomography (PET) to scan the brains of 20 healthy subjects, ranging in age from 22 to 72, after a night of rested sleep and after sleep deprivation (being awake for about 31 hours). They found beta-amyloid increases of about 5 percent after losing a night of sleep in brain regions including the thalamus and hippocampus, regions especially vulnerable to damage in the early stages of Alzheimer's disease.

In Alzheimer's disease, beta-amyloid is estimated to increase about 43 percent in affected individuals relative to healthy older adults. It is unknown whether the increase in beta-amyloid in the study participants would subside after a night of rest.

The researchers also found that study participants with larger increases in beta-amyloid reported worse mood after sleep deprivation.

"Even though our sample was small, this study demonstrated the negative effect of sleep deprivation on beta-amyloid burden in the human brain. Future studies are needed to assess the generalizability to a larger and more diverse population," said Dr. Shokri-Kojori.

It is also important to note that the link between sleep disorders and Alzheimer's risk is considered by many scientists to be "bidirectional," since elevated beta-amyloid may also lead to sleep disturbances.

https://www.sciencedaily.com/releases/2018/04/180413155301.htm

Dementia: How circadian clock controls daily rhythms of aggression

New findings shed light on the early-evening agitation known as 'sundowning,' common in patients with dementia and Alzheimer's disease

April 9, 2018

Science Daily/Beth Israel Deaconess Medical Center

Synchronized by light and darkness, the circadian clock exerts control over wake/sleep cycles, body temperature, digestion, hormonal cycles and some behavior patterns. Now, for the first time, a team of neuroscientists has demonstrated circadian control of aggression in male mice and identified the specific neurons and circuitry regulating the daily pattern. The insight opens the door to potential opportunities for managing 'sundowning,' the evening-time agitation common in patients with degenerative neurological disorders.

Now, for the first time, a team of neuroscientists at Beth Israel Deaconess Medical Center (BIDMC) has demonstrated circadian control of aggression in male mice and identified the specific neurons and circuitry regulating the daily pattern. The insight opens the door to potential opportunities for managing the evening-time agitation common in patients with degenerative neurological disorders. The study was published today in Nature Neuroscience.

"Sundowning is often the reason that patients have to be institutionalized, and if clinicians can control this circuit to minimize aggressiveness at the end of the day, patients may be able to live at home longer," said senior author Clifford B. Saper, MD, Chair of the Department of Neurology at BIDMC. "We examined the biological clock's brain circuitry and found a connection to a population of neurons known to cause violent attacks when stimulated in male mice. We wanted to know if this represented a propensity for violence at certain times of day."

Saper and colleagues observed aggressive interactions between male mice -- resident mice defending territory against intruders introduced to residents' cages at different times throughout the day. Counting the intensity and frequency of residents' attacks on intruders revealed for the first time that aggression in male mice exhibits a daily rhythm.

"The mice were more likely to be aggressive in the early evening around lights out, and least aggressive in the early morning, around lights on," Saper said. "It looks like aggressiveness builds up in mice during the lights on period, and reaches a peak around the end of the light period."

Next, the scientists used genetics-based tools to manipulate neurons known to regulate the central circadian clock. When Saper and colleagues inhibited these neurons by disabling their ability to produce a specific neurotransmitter, the mice lost the daily waxing and waning of their aggressive tendencies. These genetically manipulated mice were more aggressive overall, demonstrating a significant increase in total time attacking intruders.

Using optogenetics -- a technique that uses light to activate or deactivate targeted brain cells -- to map brain circuitry revealed two parallel pathways between the biological clock and a population of neurons in a sub-region of the hypothalamus (called the VMHvl) known to cause violent attacks when stimulated in male mice.

Taken together, the experiments showed that this circadian circuit kept aggressiveness in check in the early morning; stimulating it prevented attack, while inhibiting it promoted attack. Because stimulating the neurons in question cools off aggression, Saper suggests that controlling this circuit could potentially make animals -- and perhaps people -- less aggressive.

"Our results in mice mimic the patterns of increased aggression seen in patients during sundowning," Saper said. "This new research suggests this pathway may be compromised in neurodegenerative diseases. Examining changes to this pathway in patients could provide insight into future interventions that could greatly improve the quality of life for patients and caregivers alike."

https://www.sciencedaily.com/releases/2018/04/180409185309.htm

A heavy working memory load may sink brainwave 'synch'

April 5, 2018

Science Daily/Picower Institute at MIT

When working memory load exceeds capacity, a new study finds, feedback coupling of the prefrontal cortex with other involved regions shuts down.

Everyday experience makes it obvious -- sometimes frustratingly so -- that our working memory capacity is limited. We can only keep so many things consciously in mind at once. The results of a new study may explain why: They suggest that the "coupling," or synchrony, of brain waves among three key regions breaks down in specific ways when visual working memory load becomes too much to handle.

"When you reach capacity there is a loss of feedback coupling," said senior author Earl Miller, Picower Professor of Neuroscience at MIT's Picower Institute for Learning and Memory. That loss of synchrony means the regions can no longer communicate with each other to sustain working memory.

Maximum working memory capacity -- for instance the total number of images a person can hold in working memory at the same time -- varies by individual but averages about four, Miller said. Researchers have correlated working memory capacity with intelligence.

Understanding what causes working memory to have an intrinsic limit is therefore important because it could help explain the limited nature of conscious thought and optimal cognitive performance, Miller said.

And because certain psychiatric disorders can lower capacity, said Miller and lead author Dimitris Pinotsis, a research affiliate in Miller's lab, the findings could also explain more about how such disorders interfere with thinking.

"Studies show that peak load is lower in schizophrenics and other patients with neurological or psychiatric diseases and disorders compared to healthy people," Pinotsis said. "Thus, understanding brain signals at peak load can also help us understand the origins of cognitive impairments."

The study's other author is Timothy Buschman, assistant professor at the Princeton University Neuroscience Institute and a former member of the Miller lab.

How working memory stops working

The new study published in the journal Cerebral Cortex is a detailed statistical analysis of data the Miller lab recorded when animal subjects played a simple game: They had to spot the difference when they were shown a set of squares on a screen and then, after a brief blank screen, a nearly identical set in which one square had changed color. The number of squares involved, hence the working memory load of each round, varied so that sometimes the task exceeded the animals' capacity.

As the animals played, the researchers measured the frequency and timing of brain waves produced by ensembles of neurons in three regions presumed to have an important -- though as yet unknown -- relationship in producing visual working memory: the prefrontal cortex (PFC), the frontal eye fields (FEF), and the lateral intraparietal area (LIP).

The researchers' goal was to characterize the crosstalk among these three areas, as reflected by patterns in the brain waves, and to understand specifically how that might change as load increased to the point where it exceeded capacity.

Though the researchers focused on these three areas, they didn't know how they might work with each other. Using sophisticated mathematical techniques, they tested scores of varieties of how the regions "couple," or synchronize, at high- and low-frequencies. The "winning" structure was whichever one best fit the experimental evidence.

"It was very open ended," Miller said. "We modeled all different combinations of feedback and feedforward signals among the areas and waited to see where the data would lead."

They found that the regions essentially work as a committee, without much hierarchy, to keep working memory going. They also found changes as load approached and then exceeded capacity.

"At peak memory load, the brain signals that maintain memories and guide actions based on these memories, reach their maximum," Pinotsis said. "Above this peak, the same signals break down."

In particular, above capacity the PFC's coupling to other regions at low frequency stopped, Miller said.

Other research suggests that the PFC's role might be to employ low-frequency waves to provide the feedback the keeps the working memory system in synch. When that signal breaks down, Miller said, the whole enterprise may as well. That may explain why memory capacity has a finite limit. In prior studies, he said, his lab has observed that the information in neurons degrades as load increases, but there wasn't an obvious cut-off where working memory would just stop functioning.

"We knew that stimulus load degrades processing in these areas, but we hadn't seen any distinct change that correlated with reaching capacity," he said. "But we did see this with feedback coupling. It drops off when the subjects exceeded their capacity. The PFC stops providing feedback coupling to the FEF and LIP."

Two sides to the story

Because the study game purposely varied where the squares appeared on the left or right side of the visual field, the data also added more evidence for a discovery Miller and colleagues first reported back in 2009: Visual working memory is distinct for each side of the visual field. People have independent capacities on their left and their right, research has confirmed.

The Miller Lab is now working on a new study that tracks how the three regions interact when working memory information must be shared across the visual field.

The insights Miller's lab has produced into visual working memory led him to start the company SplitSage, which last month earned a patent for technology to measure people's positional differences in visual working memory capacity. The company hopes to use insights from Miller's research to optimize heads-up displays in cars and to develop diagnostic tests for disorders like dementia among other applications. Miller is the company's chief scientist and Buschman is chair of the advisory board.

The more scientists learn about how working memory works, and more generally about how brain waves synchronize higher level cognitive functions, the more ways they may be able to apply that knowledge to help people, Miller said.

"If we can figure out what things rhythms are doing and how they are doing them and when they are doing them, we may be able to find a way to strengthen the rhythms when they need to be strengthened," he said.

https://www.sciencedaily.com/releases/2018/04/180405093204.htm

Slow, steady waves keep brain humming

Such rhythmic waves linked to state of consciousness

March 29, 2018

Science Daily/Washington University School of Medicine

Very slow brain waves, long considered an artifact of brain scanning techniques, may be more important than anyone had realized. Researchers have found that very slow waves are directly linked to state of consciousness and may be involved in coordinating activity across distant brain regions.

If you keep a close eye on an MRI scan of the brain, you'll see a wave pass through the entire brain like a heartbeat once every few seconds. This ultra-slow rhythm was recognized decades ago, but no one quite knew what to make of it. MRI data are inherently noisy, so most researchers simply ignored the ultra-slow waves.

But by studying electrical activity in mouse brains, researchers at Washington University School of Medicine in St. Louis have found that the ultra-slow waves are anything but noise. They are more like waves in the sea, with everything the brain does taking place in boats upon that sea. Research to date has been focused on the goings-on inside the boats, without much thought for the sea itself. But the new information suggests that the waves play a central role in how the complex brain coordinates itself and that the waves are directly linked to consciousness.

"Your brain has 100 billion neurons or so, and they have to be coordinated," said senior author Marcus Raichle, MD, the Alan A. and Edith L. Wolff Distinguished Professor of Medicine and a professor of radiology at Mallinckrodt Institute of Radiology at the School of Medicine. "These slowly varying signals in the brain are a way to get a very large-scale coordination of the activities in all the diverse areas of the brain. When the wave goes up, areas become more excitable; when it goes down, they become less so."

The study is published March 29 in the journal Neuron.

In the early 2000s, Raichle and others discovered patterns of brain activity in people as they lay quietly in MRI machines, letting their minds wander. These so-called resting-state networks challenged the assumption that the brain quiets itself when it's not actively engaged in a task. Now we know that even when you feel like you're doing nothing, your brain is still humming along, burning almost as much energy daydreaming as solving a tough math problem.

Using resting-state networks, other researchers started searching for -- and finding -- brain areas that behaved differently in healthy people than in people with brain diseases such as schizophrenia and Alzheimer's. But even as resting-state MRI data provided new insights into neuropsychiatric disorders, they also consistently showed waves of activity spreading with a slow regularity throughout the brain, independently of the disease under study. Similar waves were seen on brain scans of monkeys and rodents.

Some researchers thought that these ultra-slow waves were no more than an artifact of the MRI technique itself. MRI gauges brain activity indirectly by measuring the flow of oxygen-rich blood over a period of seconds, a very long timescale for an organ that sends messages at one-tenth to one-hundredth of a second. Rather than a genuinely slow process, the reasoning went, the waves could be the sum of many rapid electrical signals over a relatively long time.

First author Anish Mitra, PhD, and Andrew Kraft, PhD -- both MD/PhD students at Washington University -- and colleagues decided to approach the mystery of the ultra-slow waves using two techniques that directly measure electrical activity in mice brains. In one, they measured such activity on the cellular level. In the other, they measured electrical activity layer by layer along the outer surface of the brain.

They found that the waves were no artifact: Ultra-slow waves were seen regardless of the technique, and they were not the sum of all the faster electrical activity in the brain.

Instead, the researchers found that the ultra-slow waves spontaneously started in a deep layer of mice's brains and spread in a predictable trajectory. As the waves passed through each area of the brain, they enhanced the electrical activity there. Neurons fired more enthusiastically when a wave was in the vicinity.

Moreover, the ultra-slow waves persisted when the mice were put under general anesthesia, but with the direction of the waves reversed.

"There is a very slow process that moves through the brain to create temporary windows of opportunity for long-distance signaling," Mitra said. "The way these ultra-slow waves move through the cortex is correlated with enormous changes in behavior, such as the difference between conscious and unconscious states."

The fact that the waves' trajectory changed so dramatically with state of consciousness suggests that ultra-slow waves could be fundamental to how the brain functions. If brain areas are thought of as boats bobbing about on a slow-wave sea, the choppiness and direction of the sea surely influences how easily a message can be passed from one boat to another, and how hard it is for two boats to coordinate their activity.

The researchers now are studying whether abnormalities in the trajectory of such ultra-slow waves could explain some of the differences seen on MRI scans between healthy people and people with neuropsychiatric conditions such as dementia and depression.

"If you look at the brain of someone with schizophrenia, you don't see a big lesion, but something is not right in how the whole beautiful machinery of the brain is organized," said Raichle, who is also a professor of biomedical engineering, of neurology, of neuroscience and of psychological and brain sciences. "What we've found here could help us figure out what is going wrong. These very slow waves are unique, often overlooked and utterly central to how the brain is organized. That's the bottom line."

https://www.sciencedaily.com/releases/2018/03/180329141012.htm

Neuroscientists say daily ibuprofen can prevent Alzheimer's disease

March 26, 2018

Science Daily/IOS Press

Neuroscientists have successfully carried out studies suggesting that, if started early enough, a daily regimen of the non-prescription NSAID (nonsteroidal anti-inflammatory drug) ibuprofen can prevent the onset of Alzheimer's disease.

A Vancouver-based research team led by Canada's most cited neuroscientist, Dr. Patrick McGeer, has successfully carried out studies suggesting that, if started early enough, a daily regimen of the non-prescription NSAID (nonsteroidal anti-inflammatory drug) ibuprofen can prevent the onset of Alzheimer's disease. This means that by taking an over-the-counter medication, people can ward off a disease that, according to Alzheimer's Disease International's World Alzheimer Report 2016, affects an estimated 47 million people worldwide, costs health care systems worldwide more than US$818 billion per year and is the fifth leading cause of death in those aged 65 or older.

The Alzheimer's Association estimates that there are more than 5 million cases in the United States alone, with a new case being identified every 66 seconds. The annual cost to the country in 2017 is estimated have been $259 billion, with that figure predicted to potentially rise to $1.1 trillion by 2050. 

Dr. McGeer, who is President and CEO of Vancouver-based Aurin Biotech, and his wife, Dr. Edith McGeer, are among the most cited neuroscientists in the world. Their laboratory is world-renowned for their 30 years of work in neuroinflammation and neurodegenerative diseases, particularly Alzheimer's disease. A paper detailing Dr. McGeer's most recent discoveries were published Friday in the Journal of Alzheimer's Disease.

In 2016, Dr. McGeer and his team announced that they had developed a simple saliva test that can diagnose Alzheimer's disease, as well as predict its future onset. The test is based on measuring the concentration of the peptide amyloid beta protein 42 (Abeta42) secreted in saliva. In most individuals, the rate of Abeta 42 production is almost exactly the same regardless of sex or age. However, if that rate of production is two to three times higher, those individuals are destined to develop Alzheimer's disease. That is because Abeta42 is a relatively insoluble material, and although it is made everywhere in the body, deposits of it occur only in the brain, causing neuroinflammation, which destroys neurons in the brains of people with Alzheimer's disease.

Contrary to the widely held belief that Abeta 42 is made only in the brain, Dr. McGeer's team demonstrated that the peptide is made in all organs of the body and is secreted in saliva from the submandibular gland. As a result, with as little as one teaspoon of saliva, it is possible to predict whether an individual is destined to develop Alzheimer's disease. This gives them an opportunity to begin taking early preventive measures such as consuming non-prescription non-steroidal drugs (NSAIDs) such as ibuprofen.

"What we've learned through our research is that people who are at risk of developing Alzheimer's exhibit the same elevated Abeta 42 levels as people who already have it; moreover, they exhibit those elevated levels throughout their lifetime so, theoretically, they could get tested anytime," says Dr. McGeer. "Knowing that the prevalence of clinical Alzheimer's Disease commences at age 65, we recommend that people get tested ten years before, at age 55, when the onset of Alzheimer's would typically begin. If they exhibit elevated Abeta 42 levels then, that is the time to begin taking daily ibuprofen to ward off the disease.

"Unfortunately, most clinical trials to date have focused on patients whose cognitive deficits are already mild to severe, and when the therapeutic opportunities in this late stage of the disease are minimal. Consequently, every therapeutic trial has failed to arrest the disease's progression. Our discovery is a game changer. We now have a simple test that can indicate if a person is fated to develop Alzheimer's disease long before it begins to develop. Individuals can prevent that from happening through a simple solution that requires no prescription or visit to a doctor. This is a true breakthrough since it points in a direction where AD can eventually be eliminated."

https://www.sciencedaily.com/releases/2018/03/180326140239.htm

Older adults who have slower walking speeds may have increased risk for dementia

March 23, 2018

Science Daily/American Geriatrics Society

Because there's currently no cure for dementia, it's important to know about risk factors that may lead to developing it. For example, researchers have learned that older adults with slower walking speeds seem to have a greater risk than those with faster walking speeds. Recently, researchers have learned more about changes in walking speed, changes in the ability to think and make decisions, and dementia.

The researchers examined information collected from the English Longitudinal Study of Aging. The study included adults aged 60 and older who lived in England. In their study, the researchers used information collected from 2002 to 2015. They assessed participants' walking speed on two occasions in 2002-2003 and in 2004-2005, and whether or not the participants developed dementia after the tests from 2006-2015. Then, they compared the people who had developed dementia with those who had not.

Researchers discovered that of the nearly 4,000 older adults they studied, those with a slower walking speed had a greater risk of developing dementia. And people who experienced a faster decline in walking speed over a two-year period were also at higher risk for dementia. People who had a poorer ability to think and make decisions when they entered the study -- and those whose cognitive (thinking) abilities declined more quickly during the study -- were also more likely to be diagnosed with dementia.

The researchers concluded that older adults with slower walking speeds, and those who experienced a greater decline in their walking speed over time, were at increased risk for dementia. But, the researchers noted, changes in walking speed and changes in an older adult's ability to think and make decisions do not necessarily work together to affect the risk of developing dementia.

https://www.sciencedaily.com/releases/2018/03/180323121747.htm

Vegetable compound could have a key role in 'beeting' Alzheimer's disease

March 20, 2018

Science Daily/American Chemical Society

A compound in beets that gives the vegetable its distinctive red color could help slow the accumulation of misfolded proteins in the brain, a process associated with Alzheimer's disease. Scientists say this could lead to the development of drugs that could alleviate some of the long-term effects of the disease, the world's leading cause of dementia.

The researchers are presenting their work today at the 255th National Meeting & Exposition of the American Chemical Society (ACS).

"Our data suggest that betanin, a compound in beet extract, shows some promise as an inhibitor of certain chemical reactions in the brain that are involved in the progression of Alzheimer's disease," says Li-June Ming, Ph.D. "This is just a first step, but we hope that our findings will encourage other scientists to look for structures similar to betanin that could be used to synthesize drugs that could make life a bit easier for those who suffer from this disease."

More than 5 million Americans have Alzheimer's disease, according to the National Institute on Aging. Its incidence rises with age, affecting one in 10 Americans 65 and older, and one in three by age 85. Scientists are still trying to figure out what causes this progressive and irreversible brain disorder. But one prime suspect is beta-amyloid, a sticky protein fragment, or peptide, that accumulates in the brain, disrupting communication between brain cells called neurons. Much of this damage occurs, Ming says, when beta-amyloid attaches itself to metals such as iron or copper. These metals can cause beta-amyloid peptides to misfold and bind together in clumps that can promote inflammation and oxidation -- a process similar to rusting -- in nearby neurons, eventually killing them.

Previous research conducted by other scientists suggests that beetroot juice can improve oxygen flow to the aging brain and possibly improve cognitive performance. Building on this work, Ming, Darrell Cole Cerrato and colleagues at the University of South Florida wanted to find out if betanin, a beet compound used in commercial dyes that readily binds to metals, could block the effects of copper on beta-amyloid and, in turn, prevent the misfolding of these peptides and the oxidation of neurons.

In laboratory studies, the researchers conducted a series of experiments involving 3,5 di-tert-butylcatechol, or DTBC, a compound that is used as a model substance for tracking the chemistry of oxidation. Using visible spectrophotometry, the scientists measured the oxidative reaction of DTBC when exposed to beta-amyloid only, beta-amyloid bound to copper, and copper-bound beta-amyloid in a mixture containing betanin.

On its own, beta-amyloid caused little or no oxidation of DTBC. However, as expected, beta-amyloid bound to copper induced substantial DTBC oxidation. But when betanin was added to the copper-bound beta-amyloid mixture, the researchers found oxidation dropped by as much as 90 percent, suggesting that misfolding of the peptides was potentially suppressed.

"We can't say that betanin stops the misfolding completely, but we can say that it reduces oxidation," Cerrato says. "Less oxidation could prevent misfolding to a certain degree, perhaps even to the point that it slows the aggregation of beta-amyloid peptides, which is believed to be the ultimate cause of Alzheimer's."

https://www.sciencedaily.com/releases/2018/03/180320084414.htm

The brain puts the memories warehouse in order while we sleep

March 15, 2018

Science Daily/FECYT - Spanish Foundation for Science and Technology

During the hours of sleep the memory performs a cleaning shift. A study reveals that when we sleep, the neural connections that collect important information are strengthened and those created from irrelevant data are weakened until they get lost.

Throughout the day, people retain a lot of information. The brain creates or modifies the neural connections from these data, elaborating memories. But most of the information we receive is irrelevant and it does not make sense to keep it. In such a case, the brain would be overloaded.

So far there have been two hypotheses about how the sleeping brain modifies the neural connections created throughout the day: while one of them argues that all of them are reinforced during sleep hours, the other maintains that their number is reduced.

A group of scientists from the Ole Paulsen Laboratory, at the University of Cambridge (United Kingdom), has analyzed the mechanisms underlying the maintenance of memory during the phase of slow wave sleep -- the third phase of sleep without rapid eye movements in the brain during which there is more relaxation and a deeper rest.

"Depending on the experiences of a person and depending on their relevance, the size of their corresponding neuronal connections changes. Those that save important information are smaller and those that store the dispensable are larger," explains Ana González Rueda, main author of the study and researcher at the MRC Laboratory of Molecular Biology (LMB) in Cambridge.

According to the expert, in the event that all these links were reinforced equally during sleep, the brain would be saturated by an extreme overexcitement of the nervous system.

In the study, published in the Neuron journal, the researchers stimulated the neuronal connections of mice subjected to a type of anesthesia that achieves a brain state similar to the slow wave sleep phase in humans.

In the words of González Rueda, the stimulation was carried out 'blindly' because the information contained in each of the links was not known. "We developed a system to follow the evolution of a specific neuronal synapse and thus study what type of activity influences that these are maintained, grow or decrease."

What isthe maintenance of neural connections dependent on?

The results show that during slow wave sleep, the largest connections are maintained while the smaller ones are lost. This brain mechanism improves the signal-to-noise ratio -- important information remains and the dispensable is discarded -- and allows the storage of various types of information from one day to the next without losing the previous data. That is, those that have already been considered relevant are kept in that state without having to reinforce them. According to González Rueda, the brain "puts order" during the hours of sleep, discarding the weakest connections to ensure stronger and consolidated memories.

"Although the brain has an extraordinary storage capacity, maintaining connections and neuronal activities requires a lot of energy. It is much more efficient to keep only what is necessary," says the expert. "Even without maintaining all the information we receive, the brain spends 20% of the calories we consume."

This research is a first indication of the electro-physiological mechanism of sleep and opens new horizons thanks to the development of a new way of studying live synaptic plasticity.

The next objective of the experts is to research the consequences of this type of brain activity for the maintenance of certain information and to analyze new phases of sleep. "In addition to the analysis of the slow wave phase, it could be interesting to know what happens in the REM phase, during which dreams occur," concludes González Rueda.

https://www.sciencedaily.com/releases/2018/03/180315110640.htm

Cueing newly learned information in sleep improves memory, and here's how

March 8, 2018

Science Daily/Cell Press

Scientists have long known that sleep is important to the formation and retention of new memories. Memory consolidation is associated with sudden bursts of oscillatory brain activity, called sleep spindles, which can be visualized and measured on an electroencephalogram (EEG). Now researchers have found that sleep spindles also play a role in strengthening new memories when newly learned information is played back to a person during sleep.

The findings provide new insight into the process of memory consolidation during sleep. They may also suggest new ways to help people remember things better, according to the researchers.

"While it has been shown previously that targeted memory reactivation can boost memory consolidation during sleep, we now show that sleep spindles might represent the key underlying mechanism," says Bernhard Staresina of the University of Birmingham in the United Kingdom. "Thus, direct induction of sleep spindles -- for example, via transcranial electrical stimulation -- perhaps combined with targeted memory reactivation, may enable us to further improve memory performance while we sleep."

Sleep spindles are half-second to two-second bursts of brain activity, measured in the 10-16 Hertz range on an EEG. They occur during non-rapid eye movement sleep stages two and three. Earlier studies had shown that the number of spindles during the night could predict a person's memory the next day. Studies in animals also linked sleep spindles to the process by which the brain makes new connections. But many questions about the link between sleep spindles and reactivated memories during sleep remained.

Staresina along with Scott Cairney at the University of York, UK, suspected that experimental reactivation of memories might lead to a surge of sleep spindles in a sleeping person's brain. To find out, they devised an experiment in which people learned to associate particular adjectives with particular objects and scenes. Some study participants then took a 90-minute nap after their study session, whereas others stayed awake. While people napped, the researchers cued those associative memories and unfamiliar adjectives.

As expected, the researchers saw that memory cues led to an increase in sleep spindles. Interestingly, the EEG patterns during spindles enabled the researchers to discern what types of memories -- objects or scenes -- were being processed.

The findings add to evidence for an important information-processing role of sleep spindles in the service of memory consolidation, the researchers say.

"Our data suggest that spindles facilitate processing of relevant memory features during sleep and that this process boosts memory consolidation," Staresina says.

This new understanding of the way the brain normally processes and strengthens memories during sleep may help to explain how that process may go wrong in people with learning difficulties, according to the researchers. It might also lead to the development of effective interventions designed to boost memory for important information.

https://www.sciencedaily.com/releases/2018/03/180308120605.htm

Omega fish oils don’t improve school children’s reading skills or memory

March 1, 2018

Science Daily/University of Birmingham

New research has found no evidence Omega-3 fish oil supplements help aid or improve the reading ability or memory function of underperforming schoolchildren.

In the second high-quality trial of its kind, published in PLOS ONE, the researchers found an entirely different result to an earlier study carried out in 2012, where omega-3 supplements were found to have a beneficial effect on the reading ability and working memory of school children with learning needs such as ADHD.

In this second study, the researchers tested children who were in the bottom quarter of ability in reading, and found that fish oil supplements did not have any or very little effect on the children's reading ability or working memory and behaviours.

The team from the Universities of Birmingham and Oxford tested 376 children aged 7-9 years old, learning to read, but in the bottom quarter in terms of their ability.

Half of the children took a daily Omega-3 fish oil supplement and the remaining children took a placebo for 16 weeks.

Their reading and working memories were tested before and after by their parents at home and teachers in school -- with no real differences found in the outcomes.

Professor Paul Montgomery, University of Birmingham, who led the research said: "We are all keen to help kids who are struggling at school and in these times of limited resources, my view is that funds should be spent on more promising interventions. The effects here, while good for a few kids, were not substantial for the many."

Dr Thees Spreckelsen, University of Oxford, Co-Author of the report added: "Fish oil or Omega-3 fatty acids are widely regarded as beneficial. However, the evidence on benefits for children's learning and behaviour is clearly not as strong as previously thought."

https://www.sciencedaily.com/releases/2018/03/180301144543.htm

Brain stimulation helps younger, not older, adults' memory

March 1, 2018

Science Daily/University of Illinois at Chicago

A study found that while the younger adults showed memory improvement from transcranial direct current stimulation, the older adults did not.

As people grow older their memory tend to get poorer, so finding ways to improve it is an important matter of investigation given the longer contemporary lifespans that people are experiencing.

Recent research has shown that stimulating the brain with a mild electric current, known as transcranial direct current stimulation, can improve memory in both younger and older adults.

In a study published online for a forthcoming special issue on the cognitive neuroscience of aging from the Journals of Gerontology: Psychological Sciences, researchers at the University of Illinois at Chicago tested these outcomes by having younger and older sets of participants -- 48 people between the ages of 18 and 35, as well as 48 adults between the ages of 60 and 79 -- try to learn information and remember 60 face-name pairs.

Some of the study participants were given stimulation, and others received sham, or fake, stimulation. Their memories were tested both immediately after stimulation and again 24 hours later to assess effects on memory the following day.

Ultimately, the researchers found that while the younger adults showed memory improvement from stimulation, the older adults did not.

"On average the amount of improvement that younger adults showed from brain stimulation was a 50 percent improvement in memory," said Eric Leshikar, UIC clinical assistant professor of psychology and corresponding author of the study. "Importantly, we found these memory improvements both immediately after stimulation, as well as after 24 hours, suggesting that brain stimulation can effectively improve memory."

The results contradict findings from previous studies that showed that a slight electoral current through the scalp had a greater effect on cognition for older adults compared to younger adults.

Leshikar says future work will look at whether using different stimulation procedures can help propel older adults to experience memory improvement.

"It very well may be that older adults may show memory improvement from stimulation, but perhaps not under the stimulation procedures we used in this study," he said.

https://www.sciencedaily.com/releases/2018/03/180301094829.htm

Largest study of its kind finds alcohol use biggest risk factor for dementia

February 20, 2018

Science Daily/Centre for Addiction and Mental Health

Alcohol use disorders are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia. This according to a nationwide observational study of over one million adults diagnosed with dementia in France.

This study looked specifically at the effect of alcohol use disorders, and included people who had been diagnosed with mental and behavioural disorders or chronic diseases that were attributable to chronic harmful use of alcohol.

Of the 57,000 cases of early-onset dementia (before the age of 65), the majority (57%) were related to chronic heavy drinking.

The World Health Organization (WHO) defines chronic heavy drinking as consuming more than 60 grams pure alcohol on average per day for men (4-5 Canadian standard drinks) and 40 grams (about 3 standard drinks) per day for women.

As a result of the strong association found in this study, the authors suggest that screening, brief interventions for heavy drinking, and treatment for alcohol use disorders should be implemented to reduce the alcohol-attributable burden of dementia.

"The findings indicate that heavy drinking and alcohol use disorders are the most important risk factors for dementia, and especially important for those types of dementia which start before age 65, and which lead to premature deaths," says study co-author and Director of the CAMH Institute for Mental Health Policy Research Dr. Jürgen Rehm. "Alcohol-induced brain damage and dementia are preventable, and known-effective preventive and policy measures can make a dent into premature dementia deaths."

Dr. Rehm points out that on average, alcohol use disorders shorten life expectancy by more than 20 years, and dementia is one of the leading causes of death for these people.

For early-onset dementia, there was a significant gender split. While the overall majority of dementia patients were women, almost two-thirds of all early-onset dementia patients (64.9%) were men.

Alcohol use disorders were also associated with all other independent risk factors for dementia onset, such as tobacco smoking, high blood pressure, diabetes, lower education, depression, and hearing loss, among modifiable risk factors. It suggests that alcohol use disorders may contribute in many ways to the risk of dementia.

"As a geriatric psychiatrist, I frequently see the effects of alcohol use disorder on dementia, when unfortunately alcohol treatment interventions may be too late to improve cognition," says CAMH Vice-President of Research Dr. Bruce Pollock. "Screening for and reduction of problem drinking, and treatment for alcohol use disorders need to start much earlier in primary care." The authors also noted that only the most severe cases of alcohol use disorder -- ones involving hospitalization -- were included in the study. This could mean that, because of ongoing stigma regarding the reporting of alcohol-use disorders, the association between chronic heavy drinking and dementia may be even stronger.

https://www.sciencedaily.com/releases/2018/02/180220183954.htm

Higher risk of dementia for adults with congenital heart disease

February 20, 2018

Science Daily/Cincinnati Children's Hospital Medical Center

A new study is believed to be the first to show a higher risk of dementia in adults who were born with heart disease. The study of more than 10,000 adult with congenital heart disease (CHD) in Denmark discovered a particularly increased risk for early dementia in middle-age adults.

"We've learned that CHD is a lifelong condition," says Nicolas Madsen, MD, a pediatric cardiologist at Cincinnati Children's Hospital Medical Center and senior author of the study. "Research shows that children born with heart problems are at a greater risk for one or more neurodevelopmental issues when compared to children without heart disease. We can now say that the risk for these types of problems continues well into adulthood."

The study is published online in Circulation, a journal of the American Heart Association.

Dr. Madsen and his colleagues at Aarhus University Hospital in Denmark studied 10,632 adults born between 1890 and 1982. The researchers used medical registries and a medical records review covering all Danish hospitals to identify adults with CHD diagnosed between 1963 and 2012.

The researchers found a 60 percent increased risk of dementia compared to the general population. The risk was 160 percent higher (2.6 times higher) when comparing those less than 65 years old.

Dr. Madsen says it is important to recognize that many of these adults were born during a time when medical and surgical interventions were more limited than they are today. Still, he says "we need to understand the healthcare needs and risk factors affecting the larger number of middle-age and older adults currently living with CHD."

CHD occurs in six to 10 of every 1,000 live births. Because these individuals are now living longer, the population of those with CHD is experiencing different neurodevelopmental issues than those previously described only in infants, children and young adults.

https://www.sciencedaily.com/releases/2018/02/180220143456.htm